Observational studyEuropean journal of neurology2025
Contribution of Polygenic Scores to Progression Independent of Relapse Activity in Multiple Sclerosis.
Observational study in European journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Relapse-associated worsening in apolipoprotein E ε4 carriers with relapsing multiple sclerosis.Journal of neurology, neurosurgery, and psychiatry · 2026Article
- Contribution of Polygenic Scores to Progression Independent of Relapse Activity in Multiple Sclerosis.European journal of neurology · 2025Observational
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDespite effective therapeutic control of relapses, many patients with multiple sclerosis (MS) experience, from the earliest phases of disease, disability accrual, which mostly occurs as progression independent of relapse activity (PIRA). In this observational study, we aimed at evaluating the genetic contribution to PIRA, using polygenic risk scores (PRS) in a cohort of 1162 Italian patients.
methodsPRS were derived from the largest multi-centric genome-wide association study on MS severity, conducted on more than 20,000 patients. The scores were computed at 5 p-value thresholds after a clumping procedure. Association with the rate of PIRA events was tested by fitting negative binomial regression models.
resultsAnalyses revealed a trend for association of PRS with the rate of PIRA events, which were significant in the subset of patients with age at onset ≤ 50 years (Rate Ratio = 1.148, 95% CI: 1.01 to 1.304, p = 0.0328). An interaction effect was identified between PRS and AAO, indicating a significant mild antagonistic effect (RR
conclusionsOur results suggest an influence of severity-related genetic load on the rate of PIRA events, especially in subjects with disease onset before the age of 50 years, characterized by a less prominent effect of aging processes on disability accumulation. This finding supports previous observations from other studies of an age-dependent influence of genetic risk scores on complex traits.
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